Enhanced semantic priming (SP) has been reported in individuals with schizophrenia who exhibit positive formal thought disorder (TD) and it has been linked to heightened automatic spreading activation in semantic networks of these patients. However, the state or trait nature of semantic hyperpriming in schizophrenia and its relation to clinical features (e.g., length of illness, symptom shifts) is not clear. To explore these issues, we administered a lexical decision task with semantically related, indirectly related or unrelated prime-target pairs to acutely ill inpatients with schizophrenia shortly after admission and again after 12-16 weeks, while most patients were already in (partial) remission (n=33). In addition, we examined 20 healthy control subjects twice (2 weeks apart). Relative to control subjects, TD patients with schizophrenia exhibited hyperpriming only in the acute psychotic state, but not during the follow-up examination, when TD and other positive symptoms had resolved. There were no associations between priming effects and length of illness or number of previous psychotic episodes. In conclusion, semantic hyperpriming in TD patients with schizophrenia appears to be clearly state-dependent and might be viewed as an episode marker of psychosis with TD.
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http://dx.doi.org/10.1016/s0920-9964(03)00066-5 | DOI Listing |
Schizophr Bull Open
January 2022
Department of Psychiatry, Institute of Mental Health and Hospital, Agra, Uttar Pradesh, India.
Neuropsychologia
December 2021
Laboratório de Neurociências (LIM-27), Faculdade de Medicina, Departamento e Instituto de Psiquiatria, Hospital das Clínicas HCFMUSP, Universidade de São Paulo, Brazil.
In this theoretical review we bridge the cognitive and neurobiological sciences to shed light on the neurocognitive foundations of the semantic priming effect in schizophrenia. We review and theoretically evaluate the neurotransmitter systems (dopaminergic, GABAergic and glutamatergic) and neurobiological underpinnings of behavioural and electrophysiological (N400) semantic priming in the pathology, and the main hypotheses on their geneses: a disinhibition of the semantic spread of activation, a disorganised semantic storage or noisy lexical-semantic associations, a psychomotor artefact, an artefact of relatedness proportions, or an inability to mobilise contextual information. We further assess the literature on the endophenotype of Formal Thought Disorder from multiple standpoints, ranging from neurophysiology to cognition: considerations are weaved on neuronal (PV basket cell, SST, VIP) and receptor deficits (DRD1, NMDA), neurotransmitter imbalances (dopamine), cortical and dopaminergic lateralisation, inter alia.
View Article and Find Full Text PDFLancet Psychiatry
June 2018
Department of Psychiatry and Psychotherapy, Marburg University, Marburg, Germany.
Formal thought disorder (FTD) is present in most psychiatric disorders and in some healthy individuals. In this Review, we present a comprehensive, integrative, and multilevel account of what is known about FTD, covering genetic, cellular, and neurotransmitter effects, environmental influences, experimental psychology and neuropsychology, brain imaging, phenomenology, linguistics, and treatment. FTD is a dimensional, phenomenologically defined construct, which can be clinically subdivided into positive versus negative and objective versus subjective symptom clusters.
View Article and Find Full Text PDFCortex
August 2015
U1077, INSERM, Caen, France; UMR-S1077, University of Caen Lower Normandy, Caen, France; UMR-S1077, Ecole Pratique des Hautes Etudes, Caen, France; U1077, University Hospital, Caen, France.
Semantic deficits are often reported in even the very early stages of Alzheimer's disease (AD), but investigations usually focus on concrete and non-emotional entities, ignoring the broad range of concepts that feature in everyday conversations. Emotional concepts (e.g.
View Article and Find Full Text PDFThere is now a large body of evidence showing that many different conditions related to impaired fronto-executive functioning are associated with the enhancement of some types of creativity. In this paper, we pursue the possibility that the central mechanism associated with this effect might be a reduced capacity to exert inhibition. We tested this hypothesis by exhausting the inhibition efficiency through prolonged and intensive practice of either the Simon or the Eriksen Flanker task.
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